The Time Course of Visual Field Recovery and Changes of Retinal Ganglion Cells after Optic Chiasmal Decompression

2011 ◽  
Vol 52 (11) ◽  
pp. 7966 ◽  
Author(s):  
Chan Hee Moon ◽  
Sun Chul Hwang ◽  
Young-Hoon Ohn ◽  
Tae Kwann Park
PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e76590 ◽  
Author(s):  
Amir H. Marvasti ◽  
Andrew J. Tatham ◽  
Linda M. Zangwill ◽  
Christopher A. Girkin ◽  
Jeffrey M. Liebmann ◽  
...  

1996 ◽  
Vol 36 (7) ◽  
pp. 913-931 ◽  
Author(s):  
Tsaiyao Yeh ◽  
Barry B. Lee ◽  
Jan Kremers

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yanghui Sheng ◽  
Lujing Chen ◽  
Xiaozhi Ren ◽  
Zheng Jiang ◽  
King-Wai Yau

AbstractIntrinsically-photosensitive retinal ganglion cells (ipRGCs) are non-rod/non-cone retinal photoreceptors expressing the visual pigment, melanopsin, to detect ambient irradiance for various non-image-forming visual functions. The M1-subtype, amongst the best studied, mediates primarily circadian photoentrainment and pupillary light reflex. Their intrinsic light responses are more prolonged than those of rods and cones even at the single-photon level, in accordance with the typically slower time course of non-image-forming vision. The short (OPN4S) and long (OPN4L) alternatively-spliced forms of melanopsin proteins are both present in M1-ipRGCs, but their functional difference is unclear. We have examined this point by genetically removing the Opn4 gene (Opn4−/−) in mouse and re-expressing either OPN4S or OPN4L singly in Opn4−/− mice by using adeno-associated virus, but found no obvious difference in their intrinsic dim-flash responses. Previous studies have indicated that two dominant slow steps in M1-ipRGC phototransduction dictate these cells’ intrinsic dim-flash-response kinetics, with time constants (τ1 and τ2) at room temperature of ~ 2 s and ~ 20 s, respectively. Here we found that melanopsin inactivation by phosphorylation or by β-arrestins may not be one of these two steps, because their genetic disruptions did not prolong the two time constants or affect the response waveform. Disruption of GAP (GTPase-Activating-Protein) activity on the effector enzyme, PLCβ4, in M1-ipRGC phototransduction to slow down G-protein deactivation also did not prolong the response decay, but caused its rising phase to become slightly sigmoidal by giving rise to a third time constant, τ3, of ~ 2 s (room temperature). This last observation suggests that GAP-mediated G-protein deactivation does partake in the flash-response termination, although normally with a time constant too short to be visible in the response waveform.


Author(s):  
Shadi Rajabi ◽  
Craig A. Simmons ◽  
C. Ross Ethier

Glaucoma, a chronic optic neuropathy, is the second most common cause of blindness, affecting 67 million people worldwide. The damage in glaucoma occurs at the optic nerve head (ONH), where the axons of the retinal ganglion cells leave the eye posteriorly. Glaucoma is frequently associated with elevated intraocular pressure (IOP), and visual field loss can be prevented by significant lowering of IOP. Hence, the role of pressure in glaucoma is important. Unfortunately, the mechanism by which pressure leads to vision loss in glaucoma is very poorly understood.


1986 ◽  
Vol 368 (1) ◽  
pp. 154-157 ◽  
Author(s):  
Peter D. Spear ◽  
Stephanie Miller ◽  
Kathleen Vielhuber ◽  
Steven E. Kornguth

2012 ◽  
Vol 12 (9) ◽  
pp. 771-771
Author(s):  
D. Pamplona ◽  
J. Triesch ◽  
C. A. Rothkopf

2019 ◽  
Author(s):  
Venkata R. M. Chavali ◽  
Naqi Haider ◽  
Sonika Rathi ◽  
Vrathasha Vrathasha ◽  
Teja Alapati ◽  
...  

AbstractGlaucoma is a group of progressive optic neuropathies that share common biological and clinical characteristics including irreversible changes to the optic nerve and visual field loss caused by death of retinal ganglion cells (RGCs). The loss of RGCs manifests as characteristic cupping or optic nerve degeneration, resulting in visual field loss in patients with Glaucoma. Published studies on in vitro RGC differentiation from stem cells utilized classical RGC signaling pathways mimicking retinal development in vivo. Although many strategies allowed for the generation of RGCs, increased variability between experiments and lower yield hampered the cross comparison between individual lines and between experiments. To address this critical need, we developed a reproducible chemically defined in vitro methodology for generating retinal progenitor cell (RPC) populations from iPSCs, that are efficiently directed towards RGC lineage. Using this method, we reproducibly differentiated iPSCs into RGCs with greater than 80% purity, without any genetic modifications. We used small molecules and peptide modulators to inhibit BMP, TGF-β (SMAD), and canonical Wnt pathways that reduced variability between iPSC lines and yielded functional and mature iPSC-RGCs. Using CD90.2 antibody and Magnetic Activated Cell Sorter (MACS) technique, we successfully purified Thy-1 positive RGCs with nearly 95% purity.


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